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The unpaired umbilical vein carries oxygen and nutrient rich blood derived from fetal-maternal blood exchange at the chorionic villi. More than two-thirds of the blood enters the liver from its inferior border, while the remainder is shunted to the inferior vena cava through the ductus venosus, whence it returns to the fetal right atrium.

Within a week of birth, the infant's umbilical vein is completely obliterated and is replaced by a fibrous cord called the round ligament of the liver (also called ligamentum teres hepatis). It extends from the umbilicus to the transverse fissure, where it joins with the falciform ligament of the liver to separate the segment 4 from 2 & 3 of the left liver lobes.

Closure of the umbilical vein usually occurs after the umbilical arteries have closed. This prolongs the communication between the placenta and fetal heart, allowing for a sort of autotransfusion of remaining blood from the placenta to the fetus.

Under extreme pressure, the round ligament may reopen to allow the passage of blood. Such recanalization may be evident in patients with cirrhosis and portal hypertension. Patients with cirrhosis experience rapid growth of scar tissue in and around the liver, often functionally obstructing nearby vessels. Vessel occlusion increases vascular resistance and therefore leads to hypertension. In portal hypertension, the vessels surrounding the liver are subjected to abnormally high blood pressure—so high, in fact, that the force of the blood pressing against the round ligament is sufficient to recanalize the structure. This leads to a condition called Caput medusae.

A newborn baby has a patent umbilical vein for at least a week after birth. This umbilical vein may be catheterised for ready intravenous access. It may be used as a site for regular transfusion in cases of erythroblastosis or hemolytic disease.